1.The relationship between the food restriction and the formation of experimental 8astric ulcer
Chinese Journal of Pathophysiology 1986;0(01):-
On the basis of Shay's ulcer model, we have studied the effects of food re. striction time on the experimental gastric ulcer in rats. The results indicat that each restricted group forms gastric ulcer after ligation of pylorus 18 hr. There are a postive correlation between the restricted time and the severity of gastric ulcer, and a negative correlation between the severity of gastric ulcer and the amount of gastric acid secretion. We suggested that Shay's ulcer model does not belong to peptic ulcer, but belonges to one of the stress ulcers. The restricted time may play an important role in the mechanism for this ulcer model.
2.Effects of Emodin and Rhubarb Polysaccharides on the Cytoplasmic Free Calcium in the Spleen Lymphocytes of Mice
Zhuhua JIN ; Xiuzhen LIN ; Delu MA
Chinese Traditional and Herbal Drugs 1994;0(08):-
Effects of emodin and rhubarb polysaccharides on the cytoplasmic free calcium in Iymphocyte of mice were studied with the latest generation fluorescent indicator Fura-2. Resultsshowed that emodin at a final concentration of 18.5 ?mol/L promotes the influx of extracellular ca2+ of lympbocytes. Polysaccharides inhibit the influx of Ca2+ aud the release of Ca2+from intracellular stores and their effects are dose dependent. Therefore, it suggests thatemodin can improve the immune function of spleen lymphocytes, but the polysaccharides caninhibit their function. This may be ouc of the theoretical evidences of the biphasic regulationeffects of rhubarb.
3.Expression of orexin A and leptin in alimentary obesity rat and its clinical significance
Yuyan ZHAO ; Lu WANG ; Dongjie MA ; Lei TIAN ; Delu ZHENG
Chinese Journal of Geriatrics 2011;30(8):684-686
Objective To evaluate the relationships of the expression of orexin A in hypothalamus with hyperleptinemia, hyperinsulinism, and hyperlipidemia in alimentary obesity rats.Methods The alimentary obesity rat model was induced by high-fat diet in Wistar rats. The levels of leptin, insulin, C-peptide, total cholesterol (TC) and triglyeride (TG) were detected by luminescent immunoassay and biochemistry enzymic method. The gene expression of orexin A in rat hypothalamus was detected by real-time PCR. The correlation between orexin A and leptin was analyzed. Results After 8 weeks of high-fat diet feeding, the body weight, Lee's index, blood glucose, TG and TC significantly increased in obesity rat group (P<0. 01). The levels of serum leptin, insulin and C-peptide were significantly higher in obesity rats than in controls [( 1.74±0. 36)μg/Lvs. (1.27±0.11) μg/L, (35±5) MIU/L vs. (23±4) MIU/L, (0.21±0.04) μg/L vs.(0. 14±0. 03) μg/L respectively, P<0.01]. However, the level of orexin A mRNA was lower in obesity rats than in controls (6.8±2.3 vs. 14.5±3.6, t=-8.06, P<0.01). The correlation coefficient (r) of orexin A mRNA with serum leptin, insulin, and C-peptide in alimentary obesity rat were -0. 726 (P<0.01), -0. 506 (P<0.01) and -0. 664 (P<0.01), respectively. Conclusions High-fat diet can induce leptin-resistance and alimentary obesity in Wistar rat. The down-regulation of orexin A in rat hypothalamus would be correlated closely to the leptin and insulin resistance in alimentary obesity.
5.Recent progress of orexin in the regulation of adrenal gland function
Xiaocen CHANG ; Yuyan ZHAO ; Delu ZHENG ; Shujing JU ; Yang SHEN ; Lina MA
Chinese Journal of Endocrinology and Metabolism 2013;(5):435-437
[Summary] The neuropeptides orexin A and orexin B are involved in numerous central regulation processes such as energy homeostasis,sleeping behaviour,and neuroendocrine activities.Orexin receptors are expressed in a variety of tissues besides the brain,adrenal gland for example.The article reviews the effect of orexin on adrenal gland function.
6.Analysis and Discussion of Clinical Features of Complete Androgen Insensitivity Syndrome Combined with Müllerian Duct Remnants
Shanjiao QIU ; Yuying XU ; Jun ZHANG ; Delu CHEN ; Cheng XU ; Huamei MA ; Juncheng LIU ; Shaobin LIN
Journal of Sun Yat-sen University(Medical Sciences) 2024;45(6):1026-1035
[Objective]To present a case of complete androgen insensitivity syndrome (CAIS) coexisting with Müllerian duct remnants (MDR) and to review previous reports in the literature to enhance the understanding of the clinical manifestations and pathophysiology of CAIS.[Methods]The study aimed to diagnose complete androgen insensitivity syndrome (CAIS) by conducting physical examinations,chromosomal analysis,whole exome sequencing,laboratory tests including follicle-stimulating hormone (FSH),luteinizing hormone (LH),total testosterone,estradiol,anti-Müllerian hormone (AMH),inhibin B,dehydroepiandrosterone sulfate (DHEAS),androstenedione,17-hydroxyprogesterone,and imaging studies such as pelvic ultrasound and pelvic magnetic resonance imaging (MRI). Laparoscopy revealed the presence of Müllerian duct structures. Additionally,the study reviewed similar cases of CAIS combined with Müllerian duct remnants reported in the literature.[Results]The child presented with female phenotype,elevated levels of FSH,LH,and testosterone. Pelvic MRI showed bilateral cryptorchidism without visible uterus or fallopian tubes. The chromosomal karyotype was 46,XY,and whole exome sequencing identified a pathogenic variant in the androgen receptor (AR) gene,c.2359C>T (p.Arg787*). No abnormalities were found in the AMH and AMHR2 gene tests. Laparoscopic exploration revealed underdeveloped testes and an underdeveloped uterus. Pathology showed the presence of fallopian tube-like structures next to the testicles. A total of 11 cases with genetically confirmed diagnosis of CAIS coexisting with MDR were retrieved from the database. The findings suggest that the initial clinical presentation,biochemical data,and gonadal pathology of CAIS with MDR are similar to those without MDR.[Conclusion]The study reports a patient with CAIS coexisting with MDR,which broadens the clinical spectrum of CAIS and provides a perspective for basic research on Müllerian duct regression that is independent of the AMH-AMHR2 signaling pathway.